Cardioprotective potential of polyphenols rich Thraatchathi Chooranam against isoproterenol induced myocardial necrosis in experimental rats

Abstract

Background The present study establishes the cardioprotective role of Thraatchathi Chooranam (TC), a polyherbal traditional Siddha medicine, in terms of membrane stabilizing and antioxidant properties in isoproterenol (ISO) induced myocardial necrosis model in rats. Methods Animals were divided into six groups (n = 6), normal (received vehicle 0.5% CMC, p.o.), ISO control (received 0.5% CMC + ISO 120 mg/kg, b.w. s.c. twice at an interval of 48 h), standard control (received Vit-E 100 mg/kg, p.o.) + ISO, TC low and high dose (50 and 100 mg/kg p.o., respectively) + ISO, and drug control (received TC at 100 mg/kg, p.o.). At the end of experimental period, blood samples collected and plasma cardiac troponin-I (CTn-I) was measured by ELISA. Cardiac tissues were isolated, levels of membrane stabilizing enzymes, antioxidants and inflammatory markers were estimated. Gene expression of Bax, Bcl2, Caspase 3, HIF-α, TNF-α, iNOS, TRX1 and TrxR were performed by RT-PCR. Histopathological studies on cardiac tissues were conducted using hematoxylin and eosin (H&E) stain. Statistical analyses were performed by one-way ANOVA followed by Tukey’s multiple comparison as post-hoc test. Results Administration of ISO resulted in a significant increase in plasma CTn-I, decrease in superoxide dismutase, glutathione and glutathione peroxidase; it also significantly altered membrane stabilizing enzymes like Na+/K+-ATPase, Mg2+-ATPase Ca2+-ATPase and Cathepsin D. Pretreatment with TC (50 mg/kg and 100 mg/kg) decreased CTn-I, and improved membrane stabilizing and endogenous antioxidant enzymes and decreased cathespin D level in a dose dependent manner. Histopathological examination revealed that TC improves cellular membrane integrity and decreases inflammatory cell infiltration and necrotic death. Conclusion The present study provided a strong evidence on the protective effects of TC against ISO-induced myocardial necrosis in rats.

Boeravinone B alleviates gut dysbiosis during myocardial infarction‐induced cardiotoxicity in rats

“…The level of NGAL is boosted in the chronic heart failure patients compared with the normal individuals. Moreover, the investigation suggests that the increased level of NGAL is related to the inflammatory reaction 5,11 . In our experimental research, it has been proved that the increased expression of NGAL improved the expression of pro‐inflammatory cytokines such as IL‐6, IL‐1β, IL‐8 and TNF‐α.…”

“…Any natural compound with good antioxidant activity is thought to protect cardiac tissues from MI. Studies suggest that ISO‐induced myocardial dysfunction in the heart of the rodent is similar to human myocardial ischaemia 4,11 . As a result, ISO is widely used to induce MI in rats to investigate the effects of different processed drugs on MI.…”

Cardioprotective Effect of Gossypin Against Myocardial Ischemic/Reperfusion in Rats via Alteration of Oxidative Stress, Inflammation and Gut Microbiota

“…It involves various changes in the signaling and metabolic pathways that are involved in enhanced oxidative stress, excessive cytoplasmic/mitochondrial calcification, irreversible DNA injury, lipid peroxidation (LPO), dynamic cellular metabolism, altered antioxidant homeostasis and pathophysiology. 6 , 7 Clinically, I/R diagnosis via observing the loss of ventricular functionality, electrocardiograph and blood pressure, coupled with boosted serum expression of cardiac-related proteins. I/R can induce other symptoms such as cardiac hypertrophy and myocardial fibrosis.…”

“…The mechanism involved in the I/R associated with inflammation, apoptosis and oxidative stress. 6 , 8 , 9 …”

“…Isoprenaline (1-[3,4-dihydroxyphenyl]-2-isopropylamino ethanol hydrochloride) is a β-adrenoceptor agonist (catecholamine drug) widely used in the treatment of bronchial asthma, allergic emergencies, ventricular bradycardia, glaucoma and cardiac arrest. 6 , 8 , 9 However, a large dose of ISO induces the stress in myocardium via reducing the energy of stored molecules in cardiomyocytes, which ultimately induces the infarcts such as irreversible cellular injury and necrosis. 10–12 After autooxidation, ISO produces a huge quantity of free radicals, altering the tissue defense systems, such as antioxidant molecules or chemical scavengers and endogenous antioxidant enzymes, such as glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT).…”